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CCL27-CCR10 interactions regulate T cell-mediated skin inflammation.

Authors
  • Homey, Bernhard1
  • Alenius, Harri
  • Müller, Anja
  • Soto, Hortensia
  • Bowman, Edward P
  • Yuan, Wei
  • McEvoy, Leslie
  • Lauerma, Antti I
  • Assmann, Till
  • Bünemann, Erich
  • Lehto, Maili
  • Wolff, Henrik
  • Yen, David
  • Marxhausen, Heather
  • To, Wayne
  • Sedgwick, Jonathon
  • Ruzicka, Thomas
  • Lehmann, Percy
  • Zlotnik, Albert
Type
Published Article
Journal
Nature medicine
Publication Date
February 2002
Volume
8
Issue
2
Pages
157–165
Identifiers
PMID: 11821900
Source
Medline
License
Unknown

Abstract

The skin-associated chemokine CCL27 (also called CTACK, ALP and ESkine) and its receptor CCR10 (GPR-2) mediate chemotactic responses of skin-homing T cells in vitro. Here we report that most skin-infiltrating lymphocytes in patients suffering from psoriasis, atopic or allergic-contact dermatitis express CCR10. Epidermal basal keratinocytes produced CCL27 protein that bound to extracellular matrix, mediated adhesion and was displayed on the surface of dermal endothelial cells. Tumor necrosis factor-alpha and interleukin-1beta induced CCL27 production whereas the glucocorticosteroid clobetasol propionate suppressed it. Circulating skin-homing CLA+ T cells, dermal microvascular endothelial cells and fibroblasts expressed CCR10 on their cell surface. In vivo, intracutaneous CCL27 injection attracted lymphocytes and, conversely, neutralization of CCL27-CCR10 interactions impaired lymphocyte recruitment to the skin leading to the suppression of allergen-induced skin inflammation. Together, these findings indicate that CCL27-CCR10 interactions have a pivotal role in T cell-mediated skin inflammation.

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